Implantable devices for pacing, cardioversion, defibrillation and resynchronization of cardiac electrical and mechanical function are widely available to prevent and treat arrhythmias and dysynchronous myocardial mechanics. These disorders can impair cardiac performance by altering electrical conduction patterns or by changing myocardial contractility or compliance, both of which result in mechanical dysfunction.
For example, conduction abnormalities may occur between the atria and the ventricular chambers. When atrio-ventricular (AV) timing is shortened, ventricular contraction may prematurely terminate the atrial kick produced by the contracting atrium. When AV timing is prolonged, increased ventricular loading from the atria may be lost due to regurgitation during prolonged diastole. Thus, both shortened and prolonged AV timing intervals can affect cardiac output.
Conduction abnormalities between right and left ventricular chambers (inter-ventricular) or within the right or left ventricles (intra-ventricular) can also result in dysynchrony. Dysynchrony occurs when forces generated in specific regions at inappropriate times cause bulging of the chamber walls into adjacent relaxed wall segments, or against prematurely closed heart valves. This lack of coordination during myocardial contraction may cause a reduction of forward blood flow and lead to reduced contractile efficiency.
Conduction abnormalities may also result in contractile and compliance abnormalities with cardiac function. For example, conduction delays may cause the left ventricular myocardium to continue to contract even after the closure of the aortic valve. This persistent contractile effect creates post-systolic wall thickening that can reduce left ventricle compliance and cause a reduction in ventricular end-diastolic volume (pre-load). The reduction in pre-load will reduce stroke volume and cardiac output through the Frank-Starling mechanism. Post-systolic wall thickening and post-systolic myocardial motion are also indicative of inefficient cardiac effort occurring against a closed aortic valve.